The study, which included five NARSAD Grantees in total, focused on a mouse model of schizophrenia that mimics the surplus of dopamine, a chemical messenger, found in the disorder. This extra dopamine is found mainly in a part of the basal ganglia, a region deep within the brain important for movement, learning and motivation. These mice have problems with learning and motivation, similar to the cognitive and negative symptoms of schizophrenia.

Researchers found that the brains of these mice had extra connections between neurons that aren’t normally connected. These “crossed wires” scrambled the activity in these neurons, leading to unexpected effects on movement. The wayward connections could be unplugged in several ways, however. For example, blocking dopamine receptors with haloperidol, an antipsychotic medication, decreased the number of connections. This is evidence of the brain’s continuing capacity to adapt―its plasticity―that may be able to be targeted and enhanced with future therapies for schizophrenia.

Other NARSAD Grantees who took part in this research study included Nao Chuhma, M.D., Ph.D., Stephen Rayport, M.D., Ph.D., and Holly Moore, Ph.D. of Columbia University and Susanne E. Ahmari, M.D., Ph.D., of the University of Pittsburgh.